Research Interests

Research summaryThe aetiology of human obstetric complications, including preeclampsia and intrauterine growth restriction (IUGR), remains largely unclear. However, one of the most widely accepted theories is that shallow invasion of extravillous trophoblasts into the endometrium results in insufficient conversion of spiral arteries, and hence malperfusion of the placenta.

I am elucidating the placental molecular mechanisms and signal transduction pathways involved in IUGR and preeclampsia. Results indicate that in IUGR the induction of endoplasmic reticulum (ER) stress plays a crucial role via activation of protein synthesis inhibition and suppression of cell proliferation. These can be mimicked in vitro by hypoxia-reoxygenation of trophoblast-like cell lines. ER stress is greater in placentas from cases of IUGR complicated by preeclampsia, leading to the induction of apoptosis. This additional component may explain the increase in circulating placental debris that is thought to cause maternal endothelial cell activation. ER stress provides a novel explanation for the pathophysiology of these diseases.

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